Abstract

C ase study: A 62-year-old male smoker with type 2 diabetes mellitus and hypertension presents with a 4-month history of exertional chest pain. Physical examination shows a blood pressure of 152/90 mm Hg but is otherwise unremarkable. The ECG is normal, and laboratory tests show a fasting blood glucose value of 110 mg/dL, glycosylated hemoglobin 6.0%, creatinine 1.1 mg/dL, total cholesterol 160, LDL 120, HDL 38, and triglycerides 147 mg/dL. He exercises for 8 minutes, experiences chest pain, and is found to have a 2-mm ST-segment depression in the inferolateral leads at the end of exercise. Chronic stable angina (CSA) is defined as the predictable occurrence with exertion or emotional upset of pressure or a squeezing sensation in the substernal area of the chest and adjacent areas1 due to transient myocardial ischemia. Anginal equivalents (exertional breathlessness, fatigue, and/or nausea) may also occur with physical activity or emotional stress. Early onset of angina during exercise after a heavy meal or in cold weather is common. Symptoms may worsen in the presence of thyrotoxicosis, tachycardia, aortic stenosis, poorly controlled hypertension, or severe anemia. An imbalance between myocardial oxygen demand and supply is the usual cause of angina resulting from myocardial ischemia. In most patients with CSA, the underlying cause is severe atherosclerotic narrowing (≥70%) of 1 or more coronary arteries, which paradoxically may constrict during exercise because of endothelial dysfunction (Figure).2–4 In addition, the coronary arteries in patients with CSA may also contain nonobstructive lesions; such non–flow-limiting plaques progress at variable rates, may remain “silent,” and may rupture unpredictably,5 manifesting as an acute coronary syndrome (myocardial infarction [MI], unstable angina [UA], or ischemic sudden death [ISD]; Figure).2–4 Pathophysiological mechanisms of myocardial ischemia and angina and of adverse outcomes in stable angina (modified with permission from Thadani …

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